ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000F23

Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease

Identifieur interne : 000F23 ( PascalFrancis/Corpus ); précédent : 000F22; suivant : 000F24

Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease

Auteurs : J. M. Wilson ; A. I. Levey ; A. Rajput ; L. Ang ; M. Guttman ; K. Shannak ; H. B. Niznik ; O. Hornykiewicz ; C. Pifl ; S. J. Kish

Source :

Neurology [ 0028-3878 ] ; 1996.

RBID : Pascal:96-0443398

Descripteurs français

Pascal (Inist)
- Parkinson maladie, Dopamine, Marqueur biologique, Corps strié, Physiopathologie, Homme, Postmortem.

English descriptors

KwdEn :
- Biological marker, Corpus striatum, Dopamine, Human, Parkinson disease, Pathophysiology, Postmortem.

Abstract

-To determine the extent that different dopamine (DA) neuronal markers provide similar estimates of striatal (caudate and putamen) DA nerve terminal loss in idiopathic Parkinson's disease (PD), we compared, in postmortem striatum of 12 patients with PD and 10 matched controls, levels of five different DA neuronal markers. These markers included DA itself, three different estimates of the density of the DA transporter (DAT) ([³H]GBR 12,935 and [³H]WIN 35,428 binding ; DAT protein immunoreactivity), and one estimate of the vesicular monoamine transporter (VMAT2 ; [³H]DTBZ binding). Striatal levels of all examined DA markers in PD were significantly intercorrelated. However, the magnitude of loss relative to controls was unequal (DAT protein = DA > [³H]WIN 35,428 > [³H]DTBZ > [³H]GBR 12,935), with the differences more marked in the severely affected putamen. The less severe reduction of binding of the DAT/VMAT2 radioligands relative to DA and DAT protein could be explained by differential regulation/degeneration of different DA nerve terminal components or lack of specificity of the radioligands for the DA neuron. These postmortem data may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 NEURAI`
A03		`1`		`@0 Neurology`
A05				`@2 47`
A06				`@2 3`
A08	`01`	`1`	`ENG`	`@1 Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease`
A11	`01`	`1`		`@1 WILSON (J. M.)`
A11	`02`	`1`		`@1 LEVEY (A. I.)`
A11	`03`	`1`		`@1 RAJPUT (A.)`
A11	`04`	`1`		`@1 ANG (L.)`
A11	`05`	`1`		`@1 GUTTMAN (M.)`
A11	`06`	`1`		`@1 SHANNAK (K.)`
A11	`07`	`1`		`@1 NIZNIK (H. B.)`
A11	`08`	`1`		`@1 HORNYKIEWICZ (O.)`
A11	`09`	`1`		`@1 PIFL (C.)`
A11	`10`	`1`		`@1 KISH (S. J.)`
A14	`01`			`@1 Human Neurochemical Pathology Laboratory, Clarke Institute of Psychiatry @2 Toronto, Ontario @3 CAN @Z 1 aut. @Z 5 aut. @Z 6 aut. @Z 8 aut. @Z 10 aut.`
A14	`02`			`@1 Department of Neurology, Emory University @2 Atlanta, GA @3 USA @Z 2 aut.`
A14	`03`			`@1 Department of Neurology, University of Saskatchewan @2 Saskatoon, Saskatchewan @3 CAN @Z 3 aut.`
A14	`04`			`@1 Department of Neuropathology, Sunnybrook Hospital @2 Toronto, Ontario @3 CAN @Z 4 aut.`
A14	`05`			`@1 Department of Molecular Neurobiology, Clarke Institute of Psychiatry @2 Toronto, Ontario @3 CAN @Z 7 aut.`
A14	`06`			`@1 Institute of Biochemical Pharmacology, University of Vienna @2 Vienna @3 AUT @Z 8 aut. @Z 9 aut.`
A14	`07`			`@1 Rotman Research Institute, Baycrest Center for Geriatric Care @2 Toronto, Ontario @3 CAN @Z 10 aut.`
A20				`@1 718-726`
A21				`@1 1996`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 6345 @5 354000066172200180`
A44				`@0 0000 @1 © 1996 INIST-CNRS. All rights reserved.`
A45				`@0 43 ref.`
A47	`01`	`1`		`@0 96-0443398`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Neurology`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 -To determine the extent that different dopamine (DA) neuronal markers provide similar estimates of striatal (caudate and putamen) DA nerve terminal loss in idiopathic Parkinson's disease (PD), we compared, in postmortem striatum of 12 patients with PD and 10 matched controls, levels of five different DA neuronal markers. These markers included DA itself, three different estimates of the density of the DA transporter (DAT) ([³H]GBR 12,935 and [³H]WIN 35,428 binding ; DAT protein immunoreactivity), and one estimate of the vesicular monoamine transporter (VMAT2 ; [³H]DTBZ binding). Striatal levels of all examined DA markers in PD were significantly intercorrelated. However, the magnitude of loss relative to controls was unequal (DAT protein = DA > [³H]WIN 35,428 > [³H]DTBZ > [³H]GBR 12,935), with the differences more marked in the severely affected putamen. The less severe reduction of binding of the DAT/VMAT2 radioligands relative to DA and DAT protein could be explained by differential regulation/degeneration of different DA nerve terminal components or lack of specificity of the radioligands for the DA neuron. These postmortem data may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.
C02	`01`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Parkinson maladie @5 01`
C03	`01`	`X`	`ENG`	`@0 Parkinson disease @5 01`
C03	`01`	`X`	`SPA`	`@0 Parkinson enfermedad @5 01`
C03	`02`	`X`	`FRE`	`@0 Dopamine @2 NK @2 FR @5 04`
C03	`02`	`X`	`ENG`	`@0 Dopamine @2 NK @2 FR @5 04`
C03	`02`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 04`
C03	`03`	`X`	`FRE`	`@0 Marqueur biologique @5 05`
C03	`03`	`X`	`ENG`	`@0 Biological marker @5 05`
C03	`03`	`X`	`SPA`	`@0 Marcador biológico @5 05`
C03	`04`	`X`	`FRE`	`@0 Corps strié @5 06`
C03	`04`	`X`	`ENG`	`@0 Corpus striatum @5 06`
C03	`04`	`X`	`SPA`	`@0 Cuerpo estriado @5 06`
C03	`05`	`X`	`FRE`	`@0 Physiopathologie @5 17`
C03	`05`	`X`	`ENG`	`@0 Pathophysiology @5 17`
C03	`05`	`X`	`SPA`	`@0 Fisiopatología @5 17`
C03	`06`	`X`	`FRE`	`@0 Homme @5 20`
C03	`06`	`X`	`ENG`	`@0 Human @5 20`
C03	`06`	`X`	`SPA`	`@0 Hombre @5 20`
C03	`07`	`X`	`FRE`	`@0 Postmortem @5 21`
C03	`07`	`X`	`ENG`	`@0 Postmortem @5 21`
C03	`07`	`X`	`SPA`	`@0 Postmortem @5 21`
C07	`01`	`X`	`FRE`	`@0 Système nerveux pathologie @5 37`
C07	`01`	`X`	`ENG`	`@0 Nervous system diseases @5 37`
C07	`01`	`X`	`SPA`	`@0 Sistema nervioso patología @5 37`
C07	`02`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 38`
C07	`02`	`X`	`ENG`	`@0 Central nervous system disease @5 38`
C07	`02`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 38`
C07	`03`	`X`	`FRE`	`@0 Encéphale pathologie @5 39`
C07	`03`	`X`	`ENG`	`@0 Cerebral disorder @5 39`
C07	`03`	`X`	`SPA`	`@0 Encéfalo patología @5 39`
C07	`04`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 40`
C07	`04`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 40`
C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 40`
C07	`05`	`X`	`FRE`	`@0 Maladie dégénérative @5 41`
C07	`05`	`X`	`ENG`	`@0 Degenerative disease @5 41`
C07	`05`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 41`
N21				`@1 303`

Format Inist (serveur)

NO :	PASCAL 96-0443398 INIST
ET :	Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease
AU :	WILSON (J. M.); LEVEY (A. I.); RAJPUT (A.); ANG (L.); GUTTMAN (M.); SHANNAK (K.); NIZNIK (H. B.); HORNYKIEWICZ (O.); PIFL (C.); KISH (S. J.)
AF :	Human Neurochemical Pathology Laboratory, Clarke Institute of Psychiatry/Toronto, Ontario/Canada (1 aut., 5 aut., 6 aut., 8 aut., 10 aut.); Department of Neurology, Emory University/Atlanta, GA/Etats-Unis (2 aut.); Department of Neurology, University of Saskatchewan/Saskatoon, Saskatchewan/Canada (3 aut.); Department of Neuropathology, Sunnybrook Hospital/Toronto, Ontario/Canada (4 aut.); Department of Molecular Neurobiology, Clarke Institute of Psychiatry/Toronto, Ontario/Canada (7 aut.); Institute of Biochemical Pharmacology, University of Vienna/Vienna/Autriche (8 aut., 9 aut.); Rotman Research Institute, Baycrest Center for Geriatric Care/Toronto, Ontario/Canada (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 1996; Vol. 47; No. 3; Pp. 718-726; Bibl. 43 ref.
LA :	Anglais
EA :	-To determine the extent that different dopamine (DA) neuronal markers provide similar estimates of striatal (caudate and putamen) DA nerve terminal loss in idiopathic Parkinson's disease (PD), we compared, in postmortem striatum of 12 patients with PD and 10 matched controls, levels of five different DA neuronal markers. These markers included DA itself, three different estimates of the density of the DA transporter (DAT) ([³H]GBR 12,935 and [³H]WIN 35,428 binding ; DAT protein immunoreactivity), and one estimate of the vesicular monoamine transporter (VMAT2 ; [³H]DTBZ binding). Striatal levels of all examined DA markers in PD were significantly intercorrelated. However, the magnitude of loss relative to controls was unequal (DAT protein = DA > [³H]WIN 35,428 > [³H]DTBZ > [³H]GBR 12,935), with the differences more marked in the severely affected putamen. The less severe reduction of binding of the DAT/VMAT2 radioligands relative to DA and DAT protein could be explained by differential regulation/degeneration of different DA nerve terminal components or lack of specificity of the radioligands for the DA neuron. These postmortem data may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.
CC :	002B17G
FD :	Parkinson maladie; Dopamine; Marqueur biologique; Corps strié; Physiopathologie; Homme; Postmortem
FG :	Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative
ED :	Parkinson disease; Dopamine; Biological marker; Corpus striatum; Pathophysiology; Human; Postmortem
EG :	Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease
SD :	Parkinson enfermedad; Dopamina; Marcador biológico; Cuerpo estriado; Fisiopatología; Hombre; Postmortem
LO :	INIST-6345.354000066172200180
ID :	96-0443398

Links to Exploration step

Pascal:96-0443398

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease</title>
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<keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term>
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<front><div type="abstract" xml:lang="en">-To determine the extent that different dopamine (DA) neuronal markers provide similar estimates of striatal (caudate and putamen) DA nerve terminal loss in idiopathic Parkinson's disease (PD), we compared, in postmortem striatum of 12 patients with PD and 10 matched controls, levels of five different DA neuronal markers. These markers included DA itself, three different estimates of the density of the DA transporter (DAT) ([<sup>3</sup>
H]GBR 12,935 and [<sup>3</sup>
H]WIN 35,428 binding ; DAT protein immunoreactivity), and one estimate of the vesicular monoamine transporter (VMAT2 ; [<sup>3</sup>
H]DTBZ binding). Striatal levels of all examined DA markers in PD were significantly intercorrelated. However, the magnitude of loss relative to controls was unequal (DAT protein = DA > [<sup>3</sup>
H]WIN 35,428 > [<sup>3</sup>
H]DTBZ > [<sup>3</sup>
H]GBR 12,935), with the differences more marked in the severely affected putamen. The less severe reduction of binding of the DAT/VMAT2 radioligands relative to DA and DAT protein could be explained by differential regulation/degeneration of different DA nerve terminal components or lack of specificity of the radioligands for the DA neuron. These postmortem data may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease</s1>
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<fC01 i1="01" l="ENG"><s0>-To determine the extent that different dopamine (DA) neuronal markers provide similar estimates of striatal (caudate and putamen) DA nerve terminal loss in idiopathic Parkinson's disease (PD), we compared, in postmortem striatum of 12 patients with PD and 10 matched controls, levels of five different DA neuronal markers. These markers included DA itself, three different estimates of the density of the DA transporter (DAT) ([<sup>3</sup>
H]GBR 12,935 and [<sup>3</sup>
H]WIN 35,428 binding ; DAT protein immunoreactivity), and one estimate of the vesicular monoamine transporter (VMAT2 ; [<sup>3</sup>
H]DTBZ binding). Striatal levels of all examined DA markers in PD were significantly intercorrelated. However, the magnitude of loss relative to controls was unequal (DAT protein = DA > [<sup>3</sup>
H]WIN 35,428 > [<sup>3</sup>
H]DTBZ > [<sup>3</sup>
H]GBR 12,935), with the differences more marked in the severely affected putamen. The less severe reduction of binding of the DAT/VMAT2 radioligands relative to DA and DAT protein could be explained by differential regulation/degeneration of different DA nerve terminal components or lack of specificity of the radioligands for the DA neuron. These postmortem data may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.</s0>
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<server><NO>PASCAL 96-0443398 INIST</NO>
<ET>Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease</ET>
<AU>WILSON (J. M.); LEVEY (A. I.); RAJPUT (A.); ANG (L.); GUTTMAN (M.); SHANNAK (K.); NIZNIK (H. B.); HORNYKIEWICZ (O.); PIFL (C.); KISH (S. J.)</AU>
<AF>Human Neurochemical Pathology Laboratory, Clarke Institute of Psychiatry/Toronto, Ontario/Canada (1 aut., 5 aut., 6 aut., 8 aut., 10 aut.); Department of Neurology, Emory University/Atlanta, GA/Etats-Unis (2 aut.); Department of Neurology, University of Saskatchewan/Saskatoon, Saskatchewan/Canada (3 aut.); Department of Neuropathology, Sunnybrook Hospital/Toronto, Ontario/Canada (4 aut.); Department of Molecular Neurobiology, Clarke Institute of Psychiatry/Toronto, Ontario/Canada (7 aut.); Institute of Biochemical Pharmacology, University of Vienna/Vienna/Autriche (8 aut., 9 aut.); Rotman Research Institute, Baycrest Center for Geriatric Care/Toronto, Ontario/Canada (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 1996; Vol. 47; No. 3; Pp. 718-726; Bibl. 43 ref.</SO>
<LA>Anglais</LA>
<EA>-To determine the extent that different dopamine (DA) neuronal markers provide similar estimates of striatal (caudate and putamen) DA nerve terminal loss in idiopathic Parkinson's disease (PD), we compared, in postmortem striatum of 12 patients with PD and 10 matched controls, levels of five different DA neuronal markers. These markers included DA itself, three different estimates of the density of the DA transporter (DAT) ([<sup>3</sup>
H]GBR 12,935 and [<sup>3</sup>
H]WIN 35,428 binding ; DAT protein immunoreactivity), and one estimate of the vesicular monoamine transporter (VMAT2 ; [<sup>3</sup>
H]DTBZ binding). Striatal levels of all examined DA markers in PD were significantly intercorrelated. However, the magnitude of loss relative to controls was unequal (DAT protein = DA > [<sup>3</sup>
H]WIN 35,428 > [<sup>3</sup>
H]DTBZ > [<sup>3</sup>
H]GBR 12,935), with the differences more marked in the severely affected putamen. The less severe reduction of binding of the DAT/VMAT2 radioligands relative to DA and DAT protein could be explained by differential regulation/degeneration of different DA nerve terminal components or lack of specificity of the radioligands for the DA neuron. These postmortem data may help in interpretation of in vivo neuroimaging studies in PD in which only one radioligand is routinely employed.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Dopamine; Marqueur biologique; Corps strié; Physiopathologie; Homme; Postmortem</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>Parkinson disease; Dopamine; Biological marker; Corpus striatum; Pathophysiology; Human; Postmortem</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Parkinson enfermedad; Dopamina; Marcador biológico; Cuerpo estriado; Fisiopatología; Hombre; Postmortem</SD>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease

Differential changes in neurochemical markers of striatal dopamine nerve terminals in idiopathic Parkinson's disease

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